Glicentin which is one of enteroglucagons is a peptide comprising 69 amino acid residues. For example, human glicentin is composed of the following amino acid sequence (SEQ ID NO: 1)
Arg-Ser-Leu-Gln-Asp-Thr-Glu-Glu-Lys-Ser-Arg-Ser-Phe-Ser-Ala-Ser-Gln-Ala-Asp -Pro-Leu-Ser-Asp-Pro-Asp-Gln-Met-Asn-Glu-Asp-Lys-Arg-His-Ser-Gln-Gly-Thr-Ph e-Thr-Ser-Asp-Tyr-Scr-Lys-Tyr-Leu-Asp-Ser-Arg-Arg-Ala-Gln-Asp-Phe-Val-Gln-T rp-Leu-Met-Asn-Thr-Lys-Arg-Asn-Arg-Asn-Asn-Ile-Ala
Glicentin was isolated and purified from porcine intestine by F. Sundby et al in 1976 (F. Sundby et al, Horm. Metab. Res. 8 (1976) 366-371). The structure of glicentin has been established by A. J. Moody et al (L. Thim and A. J. Moody, Regul. Pept. 2 (1981) 139-150).
It has been difficult to study human glicentin using its purified product, since the human organs such as gastrointestinal tracts were difficult to obtain in large quantities.
Now, the present inventors were successful in synthesizing DNA corresponding to the amino acid sequence of human glicentin which was deduced by G. I. Bell (Nature, 304, 368-371 (1983)) from the sequence of human preproglucagon gene and preparing human glicentin by means of genetic engineering procedure using the synthesized DNA which was disclosed in Japanese Patent Kokai Hei 4-364199. This results in easy availability of human glicentin as its purified product in large amounts.
Butylscopolamine bromide injections have been used as the agents for temporarily suppressing the motor activity of gastrointestinal tracts in the medical examinations of the digestive tracts, such as gastrointestinal roentgenologic examination and endoscopic examination. However, such butylscopolamine bromides have the effect on the systemic autonomic nervous system, thus leading to the disadvantages of bringing about side effects such as thirst, dizziness and ataxia. Further, there is glucagon as peptidic agents for suppressing the motor activity of gastrointestinal tracts. However, such glucagon is not a suitable agent, because of its unfavorable action to induce a sudden rise in blood glucose.